Сторінка 1 від 995 результати
Our previous study demonstrated that p53 plays an orchestrating role in the vasospasm and apoptotic cell death after subarachnoid hemorrhage (SAH). We now hypothesize that p53 also plays an important role in brain edema by up-regulating the expression of MMP-9 via the NF-kappaB molecular signaling
OBJECTIVE
Severe neurogenic pulmonary edema (NPE) can occur in a variety of brain insults, including subarachnoid hemorrhage (SAH), and severe case of NPE can cause devastating consequences. But the literature on the treatment strategy about aneurysmal SAH with NPE is very scant. We present that SAH
Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema after a significant central nervous system (CNS) insult. NPE occurs as a result of release of catecholamines into the blood immediately after aneurysm rupture. The aim of this study is to
Volume management is critical for assessment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). This multicenter prospective cohort study compared the impact of surgical clipping versus endovascular coiling on postoperative hemodynamics and pulmonary edema in patients with SAH.
Despite the fact that cerebral edema appears to be a common complication of subarachnoid hemorrhage (SAH) due to a ruptured cerebral aneurysm, measurements of brain tissue water content have not been carried out in this entity. For this reason, the development of cerebral edema has been analized in
Neurogenic pulmonary edema (NPE) is observed in cerebral injuries and has an impact on treatment results, being a predictor of fatal prognosis. In this study we retrospectively reviewed medical records of 250 consecutive patients with aneurysmal subarachnoid hemorrhage (SAH) for the frequency and
A 48-year-old male and a 39-year-old female presented with subarachnoid hemorrhage (SAH) due to ruptured anterior communicating artery aneurysms. Both patients were comatose on admission. Chest radiography disclosed pulmonary edema. They were conservatively treated under controlled ventilation, but
OBJECTIVE
Neurogenic pulmonary edema (NPE) is a well-known complication of subarachnoid hemorrhage (SAH), which potentially causes a poor outcome. The aim of this study was to examine if NPE occurs in the endovascular perforation model of SAH in mice and if apoptosis contributes to NPE development
OBJECTIVE
Few studies have described the risk factors associated with the development of neurological pulmonary edema (NPE) after subarachnoid hemorrhage (SAH). We have hypothesized that acute-phase increases in serum lactate levels are associated with the early development of NPE following SAH. The
Patients sustaining aneurysmal subarachnoid hemorrhage (aSAH) can be further complicated by neurogenic pulmonary edema (NPE) and Takotsubo-like cardiomyopathy (TCM) with dismal outcomes. The present study aimed to validate the efficacy of endovascular therapy for patients with aSAH Neurogenic pulmonary edema (NPE) is a well-known complication of acute central neurologic injury, particularly aneurysmal subarachnoid hemorrhage. Both increased intracranial pressure and severe over-activation of the sympathetic nervous system seem to be pathogenetic for the onset of NPE. Although
Central salt wasting syndrome may be caused by pathological increases in serum natriuretic peptides after subarachnoid hemorrhage (SAH). However, it is unclear as to why the serum concentration of atrial natriuretic peptide (ANP) or brain natriuretic peptide (BNP) increases in the subacute phase of
Vascular endothelial growth factor (VEGF) has been implicated in the pathogenesis of brain edema formation after experimental subarachnoid hemorrhage (SAH). In this study, we evaluated the effect of anti-VEGF antibody neutralization on brain edema formation after experimental SAH in mice. Mice
Aneurysmal subarachnoid hemorrhage is a life-threatening event that can cause permanent disability. This life-threatening event can be further complicated by subsequent cardiac and pulmonary disability. The presence of a neurogenic cardiomyopathy and pulmonary edema increases the morbidity and
We describe a 72-year-old woman with hypertension who developed acute neurogenic pulmonary edema and giant negative T waves on electrocardiography (ECG) due to subarachnoid hemorrhage. The patient was alert and complained of precordial chest discomfort, dyspnea and shoulder stiffness.